Failure of a Dacron or polytetrafluoreoethylene (PTFE) vascular prosthesis (VP) often occurs because distal intimal hyperplasia (DIH) of the host vessel downstream from the VP causes vessel narrowing, flow reduction, and eventual thrombosis of the VP. Canine and primate studies have implicated the interaction of blood platelets with the VP surface as a cause of DIH. These experiments suggest that prosthesis-platelet interaction leads to release of granules and platelet derived growth factors which is mitogenic for vascular wall smooth muscle and may thus exacerbate both DIH and downstream progression of atherosclerotic disease. Autologous endothelial seeding (AES) of VP produces a confluent lining of living vascular endothelial cells on VP in dogs. We have shown that this sharply curtails platelet-VP interactions, restores normal platelet survival patterns, and eliminates VP-induced platelet dense granule release. This study will use the canine model to test the hypothesis that reduction of VP-induced platelet granule release will reduce DIH at sites downstream from a seeded VP. To do this we will measure the severity of DIH at the site of balloon-catheter intimal injury in the external iliac artery. Initial studies will compare severity of DIH at the injury site with and without a proximal VP of PTFE from the thoracic to the infrarenal aorta. The second part of this experiment will utilize dogs with AES grafts which in experimental animals having an endothelial seeded VP will be compared to control animals having an unseeded VP. Platelet serotonin levels will be measured preoperatively as well as prior to balloon catheter injury and prior to sacrifice as a measure of platelet granule release. The severity of DIH measured by computer planimetry of vessel cross sections will be tested for correlation with the degree of endothelial coverage of the VP and with platelet serotonin depletion. The use of noncontiguous injury site far downstream from the distal anastomosis of the VP will allow study of the role of blood-borne platelet derived mitogens in causing DIH by avoiding sites of flow disturbance and operative injury of the vessel at or near the distal anastomosis.